Figure 2 (IMAGE)
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Signaling, mitochondrial functions, and senescence affected by aging and adipocyte-specific Crtc2 knockout. Adipocyte-specific Crtc2 knockout mice (Crtc2 AKO) resulted in a block of decreased BCAA catabolism (A), activation of mTORC1 (B), diminished mitochondrial functions (C), and the adipocyte senescence (D) caused by aging, effectively preventing the generation of aging-related adipocyte dysfunctions.
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